Hypersensitivity and Autoimmunity Flashcards Preview

Principles of Disease > Hypersensitivity and Autoimmunity > Flashcards

Flashcards in Hypersensitivity and Autoimmunity Deck (54)
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1

What cells are involved in innate immunity

Phagocytes
Eosinohpils
Basophils
Mast cells
APCs

2

What receptors are involved in innate immunity

Fc
Complement
Toll-like
Mannose
Cytokine

3

What molecules are involved in innate immunity

Complement
Acute phase reactants
Inflammatory mediators
Cytokines

4

What cells are involved in adaptive immunity

B cells
T cells

5

What receptors are involved in adaptive immunity

Ig
TCR
HLA
Cytokine
Complement
Toll-like

6

What molecules are involved in adaptive immunity

Immunoglobulins
Cytokines

7

What does immunity involve

Recognition
Interaction
Response
Elimination
Control and regulation

8

What is hypersensitivity

A group of disorders where the normally beneficial components of the immune response act in an exaggerated or inappropriate fashion to environmental antigens which do not normally cause tissue damage.

9

What is responsible for the tissue damage caused by hypersensitivity

The exaggerated response directed at the antigen

10

How can humans come into contact with allergens

Inhaled
Ingested
Injected
Contact

11

Describe the pathogenesis of an allergen

Allergen leaches on cell
Enters to form APC which has MHC, a class II protein and epitope
T helper cell helps B cells
IgE produced
IgE binds to inflammatory cell
Causes clinical effects

(Allergen could attach straight to Fc epsilon receptor to cause a response)

12

What can T helper CD4 cells form

Th 1 - found in type IV (IL-2, gamma-IFN, TNF)
Th2 - found in type I (IL-4,6,10,13)

13

Define Atopy

A genetic tendency to produce IgE to normally innocuous, common environment allergens

14

How many people does atopy affect

About 40% of the population

15

Define allergy

A clinical expression of the atopic tendency

16

How many people does allergy affect

15-20% of the population

17

State some specifc IgE triggers

Insect venom
Pollen
Mould spores
Animal dander
Food allergens

18

State some non-specific allergy and atopy triggers

Exercise
Acetylsalicylic acid
Tobacco
Sulphur dioxide
Cold air
Temperature
Pressure
Water
Food items

19

What are some of the symptoms of allergy and atopy

Anaphylaxis
Asthma
Rhinitis and conjunctivitis
Urticaria
Gastrointestinal

20

What can cause allergy

Genes
Environment (allergen)
Immune dysregulation
Environment (other)
Internal influences

21

What types of mast cell mediators are there

Preformed
Newly synthesised

22

Name some preformed mast cell mediators

Histamine
Heparin
Tryptase
Chymase
Eosinophil/neutrophil chemotactic factors

23

Name some newly synthesised mast cell mediators

Prostaglandins
Leukotrienes

24

Describe the pathogenesis of type I hypersensitivity

Allergen exposure trigger mast cells and IgE
This causes degranulation of preformed mediators and synthesis of new mediators
Response includes: mucosal oedema, secretions, vasodilation, capillary leakage and smooth muscle contraction.

25

When does an early phase response occur

Within minutes using preformed mast cell mediators

26

When does a late phase response occur

Takes hours using newly synthesised mediators, Th2 cytokines and eosinophil mediators

27

Describe type II hypersensitivity

IgG/IgM mediated and its target antigens are either found on the cell surface or fixed in certain tissues
Involves immune effectors/target cell interactions

28

How can tissue damage arise in type II hypersensitivity

Complement activation
Fc binding of immunogloubin and stimulation of phagocytes
Antibody-dependent cellular cytotoxicity (ADCC)
Effects on target cell function (inhibition of function or stimulation)

29

What is the function of the immune complex

When formed under normal/physiological conditions has protective mechanisms including opsonisation, transportation and destruction

When formed under pathological conditions it has antigen factors and host response factors

30

How can the immune complex form

In circulation causing systemic deposition in tissues (serum sickness)
Locally in tissues (arthus reaction)